Cutting Edge: Direct Interaction of TLR4 with NAD(P)H Oxidase 4 Isozyme Is Essential for Lipopolysaccharide-Induced Production of Reactive Oxygen Species and Activation of NF-κB1
By H. Park, H. Jung, E. Park, Jaesang Kim, W. Lee, Y. Bae. Journal of Immunology, 2004
666 citations recorded by the source corpus.
Subfields: Cancer Research, Immunology
View Paper: https://www.semanticscholar.org/paper/29f034878846eebf14faf832bfc327166f52ea56
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Citations in the corpus
- Nox family NADPH oxidases: Molecular mechanisms of activation. (2014, background): “and TLR4 has been reported as well as an acute increase in ROS formation by Nox4 in this model [170].”
- Radical-free biology of oxidative stress. (2008, background): “10) Similarly, mitochondrial and nonmitochondrial production of H2O2 in response to LPS activation of Toll-like receptor-4 provides additional sites of redox sensitivity (77, 139).”
- Ferroptosis in infection, inflammation, and immunity (2021, background): “In addition to its immunomodulatory roles, TLR4 may also directly promote cell death (including apoptosis and ferroptosis) by binding to NOX4 or its isoenzymes (Park et al., 2004).”